Introduction
As the triceps surae descends toward the heel it enters a broad aponeurosis. From the musculotendinous junction, the tendon gradually becomes rounded, approximately 4 cm above the calcaneus, where the tendon fibers spiral laterally through 90°. The tendo Achillis (TA) connects the triceps surae distally to the middle one-third of the posterior surface of the calcaneus. This enables the forces produced by the triceps surae to be transmitted to the hindfoot1.
Macroscopically the TA is composed of multiple fibers, which in turn are composed of fibrils; this structure enables the tendon to resist high tensile forces with minimal loss of energy and deformation (Figure 16.1). However, when considering mechanisms of injury and rehabilitation it is also important to consider that tendons are viscoelastic tissues. As such they display decreased stress with time under constant deformation (stress relaxation) and increased deformation with time under constant load (creep). Finally, the tension generated across the tendon is also dependent on the type of muscle contraction, eccentric loads producing the highest, followed by concentric, and finally isometric muscle contractions2–5.
Figure 16.1 The stress–strain curve of tendon.
Epidemiology and Etiology
The TA is the most commonly ruptured tendon in the human body and the incidence is rising6–7. European figures show approximately 18 per 100 000 people per year sustain the injury8. The pattern of incidence displays a bimodal distribution according to age, with the first peak consisting of men aged 30 to 40 years and the second women aged 60 to 80 years7–8.
From Figure 16.1 one would expect all TA ruptures, “macroscopic failures,” to occur during forced and unexpected dorsiflexion of the ankle, for example in a fall or road traffic accident. Nevertheless, both of the cohorts outlined above most commonly sustain TA ruptures below the threshold of macro-failure9. The explanation for this is widely accepted to be that ruptures occur on a background of preexisting abnormalities in the tendon resultant on tendinopathy10.
People with tendinopathy can be symptomatic, experiencing pain on loading activities, or asymptomatic. In either case the tendon displays characteristic features of tendinopathy on a cellular level, these include decreased cellularity, abnormal matrix organization, neovascularization, and increased type III collagen11. These features occur as a result of an imbalance between the protective/regenerative functions within the tendon; MMPs are thought to have a key role but the exact mechanisms are not fully understood11. These changes in the tendon structure predispose to TA rupture.
While both the younger and older groups of patients sustain tendon ruptures on a background of tendinopathy, they have contrasting mechanisms of injury. The “typical” injury of a 30- to 40-year-old male is during participation in sport, and occurs during eccentric loading of the tendon, such as sprint starts, landing from a jump, and lunging – actions typical in football and racquet sports7. In contrast the “typical” injury for a 60- to 80-year-old female occurs during normal daily activities, such as climbing stairs7. With an aging population it is this second cohort that is largely responsible for the rising incidence7.
Classification
Acute Musculotendinous Junction Rupture
Ruptures of the TA that occur in the region of the aponeurosis are classified as musculotendinous junction ruptures. As the name suggests, these injuries involve both the tendon and the muscle. Consequently, ruptures at this level may not have the characteristic palpable gap, but may have increased bruising and severe pain due to the muscle involvement12.
Acute Midsubstance Rupture
Midsubstance TA ruptures are defined as those occurring approximately 2 to 6 cm above the tendon insertion, at the point where the tendon is most rounded and the tendon fibers spiral through 90°. In contrast to musculotendinous junction ruptures, midsubstance ruptures are characterized acutely by a defined palpable gap13.
Acute Insertional Rupture
Insertional TA ruptures occur in the distal 2 cm of the tendon and involve the attachment to the os calcis. Insertional injuries may be more difficult to diagnose, as the palpable gap noted in midsubstance injuries is far less obvious. However, in the acute situation, the patient can usually localize the pain to the distal 2 cm of the tendon.
Chronic Rupture
There is a lack of consensus as to the exact time frame during which a ruptured TA is considered “chronic,” although any presentation after the first two weeks is more difficult to diagnose14. The patient will usually describe an eccentric loading injury followed by pain and a limp, so the history can be more informative than the clinical findings. Rarely, the patient cannot recall an exact event.
Presentation
Acute Rupture
The patient typically presents with a sudden pain in the area of the TA13. The most common comment made by the patient during the subjective history is a feeling that they have been “kicked in the back of the leg”13. During the objective assessment physical findings include a positive “calf-squeeze test,” decreased ankle plantar flexion strength, presence of a palpable gap, and increased ankle dorsiflexion on dorsiflexion of the ankle by the examiner13. The only published guidelines on this topic have been produced by the American Academy of Orthopaedic Surgeons (AAOS) who concluded that based on current literature there was strong evidence to support a diagnosis of a midsubstance TA rupture based on two of these four physical findings.
Chronic
The diagnosis of chronic rupture of the TA is more complicated than that of acute ruptures14. Firstly, the patient often does not present with pain and the clinical findings are more subtle. In contrast to the presentations of an acute rupture, this group of patients is more likely to report reduced power during activities that require greater “push-off” strength, for example walking upstairs or climbing a ladder. They may also report instability of the ankle, altered walking patterns, or a lack of balance.
A TA rupture that is not treated acutely will often “heal” with scar tissue filling the gap, therefore a palpable gap is rarely felt. Nevertheless on occasion palpation may identify a change in tissue consistency at the site of rupture. Additional physical findings will be largely due to the functional length of the healed tendon: commonly increased passive dorsiflexion, decreased plantar flexion power, and plantar flexion fatigue on repeated activity14.
Investigations
For acute TA ruptures, the diagnosis is usually clinical, although US may be used to identify the exact location of the rupture or in cases where the diagnosis is uncertain. The routine use of US, MRI, or radiographs in the diagnosis of TA ruptures is not supported by the current literature13. Imaging in the diagnosis of chronic TA ruptures can provide confirmation, where uncertainty exists14.
Dynamic US assessment has been suggested to be of value as a selection tool for which treatment pathways patients should be directed toward15. Such studies have used this assessment to determine if retracted torn tendon ends can be approximated on plantar flexion. However, the literature on this topic is not definitive, consequently dynamic US is not routine practice for most centers, as shown in a recent UK survey of current practice16.
Non-Operative Treatment
Non-operative management options fall into three categories: plaster cast immobilization, combined plaster cast and functional bracing, or functional bracing alone16. There is no consensus in the literature regarding an exact protocol for these categories, so the following discussion is based on a recent survey of UK practice carried out by the British Orthopaedic Foot and Ankle Society16.
Plaster cast immobilization involves an initial plaster cast applied in the “gravity equinus” position; this is the position that the foot naturally adopts when unsupported. Full equinus is avoided as this may lead to stiffness and gait abnormalities17. Once in plaster the patient is often advised not to bear weight; in fact the equinus position of the cast precludes normal weight bearing. Over a period of approximately two months, as the tendon heals, the position of the plaster cast is changed at two-week intervals until the foot is plantigrade. Patients gradually begin to introduce weight bearing. After two months the cast is removed and the patient is clinically evaluated for any signs that the tendon is not in continuity. As long as the TA heals in continuity the patient is referred for physiotherapy.
Plaster-cast immobilization combined with functional rehabilitation involves the same initial plaster-cast treatment; however, after approximately one month the cast is exchanged for a functional weightbearing brace. The functional weightbearing brace often mimics the more traditional serial casting, with return of the foot to plantigrade, but using heel raise inserts inside the brace so that the foot plate of the brace is flat to the floor, despite the ankle being plantar flexed. There are two basic designs of brace: rigid rocker bottom style (Figure 16.2) or the more flexible carbon-fiber dorsal brace18 (Figure 16.3). The flexible brace generally allows a greater range of movement than the more rigid designs. This increased, but controlled, movement has been suggested as being beneficial to tendon healing. Obviously increased flexibility must be weighed up against the possible complications of the tendon healing in a lengthened position or tendon re-rupture18.
Figure 16.2 A rocker bottom style brace, for the treatment of tendo Achillis rupture. The wedges (a) are fitted into the boot (b), which is completed with an anterior shell. The wedges are then sequentially removed, bringing the foot to neutral.
Figure 16.3 An alternative to the rocker bottom boot, a flexible dorsal brace that is worn with heel wedges, as shown in Figure 16.2a.
Functional bracing alone involves the immediate use of the brace, with either heel inserts or fixing the brace in plantar flexion and allowing immediate weight bearing. As with the two methods described above, the brace is worn for approximately two months, with the ankle gradually being moved to plantigrade, with the removal of heel inserts or adjustment of the brace settings.
This range of protocols exemplifies the complexity of this early rehabilitative intervention. For this reason synthesis of the literature comparing different rehabilitation protocols is a challenge19. Saleh et al. in 199220 were the first authors to publish a randomized controlled trial (RCT) comparing different conservative management protocols. However, the trials in this area have been small, with no definitive conclusions, as outlined in the AAOS guidelines13.
Surgical Treatment
Acute Musculotendinous Junction Rupture
As a result of the anatomy of the musculotendinous junction, there is a consensus that operative management is unnecessary – it is very difficult to achieve an adequate surgical repair when the muscle, which does not satisfactorily hold sutures, is involved12.
Acute Midsubstance Rupture
Surgical management can be broadly divided into open or percutaneous techniques, with or without augmentation8.
Open longitudinal repair involves an incision just medial to the TA, to avoid the sural nerve, and provides a clear view of the retracted tendon, which is sutured end to end8. Percutaneous repair techniques vary, but generally involve several small incisions on either side of the tendon rupture, with sutures then being blindly passed through the tendon ends, as first described by Ma and Griffith21.
The first RCT to compare open with percutaneous techniques was published by Schroeder et al. in 199722, followed by three further RCTs in 2001, 2008, and 200923–25. The main advantage of the percutaneous method is reduced infection and wound complication rates. However, this proposed advantage needs to be weighed against the risks, which include an increase in sural nerve injury8. With regard to functional outcomes, the literature remains inconclusive; nevertheless, the trend is toward percutaneous or “mini-open” surgical repair with transverse rather than longitudinal incisions.
The question as to whether to augment the repair remains. Autogenous options include primary augmentation with tendon transfer from the plantaris, peroneus, gracilis, flexor hallucis longus, flexor digitorum longus, free-grafts with hamstrings, or a gastrocnemius fascial turndown flap14. However, these all share the problem of donor-site morbidity. Synthetic grafts have therefore been suggested as an alternative, including polyester tape, Marlex® mesh, and carbon fiber, but as with all synthetic grafts there is always the risk of an immune response28. The most recent Cochrane Review identified only two RCTs26–27, consequently augmentation has not been adopted in routine practice.
Acute Insertional Rupture
Surgical repair of these injuries is complicated by the fact that there is very little, if any, tendon distal to the rupture. While the proximal end of the tendon can usually be brought down to the heel using a standard tendon suture technique, the distal end is seldom amenable to this approach, and transosseous sutures or bone anchors are usually required to achieve satisfactory distal fixation. An alternative is to use the flexor hallucis longus either through a bone tunnel or attached to the bone with anchors, if the fixation is tenuous or the TA has retracted.
Chronic Rupture
There is no consensus as to when a TA rupture becomes chronic, although four weeks is often quoted. Pragmatically, if the gap is difficult to bridge alternative strategies to simple end-to-end suture will need to be considered. Kuwada classified ruptures according to the gap found at the time of surgery, recommending different operative techniques based on the size of the defect. However, as there is no evidence to suggest that such a classification system improves outcome, it is largely accepted that management should be on a case-by-case basis, with the technique used depending on surgical preference, clinical examination, and patient factors14.
Following the decision to operate on a chronic rupture, the technique is liable to be open, rather than percutaneous, as it is necessary to mobilize the tendon ends to approximate them as closely as possible, or to introduce bridging material into the gap. After a year or so a neotendon often forms, which can closely resemble the normal tendon, although on close examination it will be noted to be homogeneous, without the fibrillar structure of the normal TA. Simple end-to-end repairs are often not possible, and therefore chronic tendon repairs frequently require augmentation. Local tissue, local tendons, and allografts can be used to reconstruct the tendon. The FHL tendon is convenient. It lies anterior to the TA, is the second strongest plantar flexor of the foot, after the gastrocnemius–soleus, and it works in phase with the triceps surae. The FHL can be harvested short, behind the ankle, or long, in the foot, depending on the length of graft required. There may be weakness of flexion of the interphalangeal joint of the great toe, although this is well tolerated. Transfer of the FHL has become the workhorse for reconstructing the late-presenting TA rupture in many surgical practices.
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